The group was initially interested in the effect of potassium, not ammonium. But their microarray data suggested that low potassium is harmful to yeast because ammonium—a similarly sized and charged ion—seeps in through the battery of induced potassium channels.

The yeast protect themselves from the intracellular ammonium by incorporating it into amino acids that they then secrete into the medium. Export seems to be through passive channels that also take up amino acids. The export may help natural yeast strains survive on ammonium-rich rotting vegetation (in which the external source of amino acids is probably also handy later on). Standard laboratory media have very high potassium levels that apparently masked ammonium's toxic effects on yeast before now.

The initial cellular response to high ammonium—converting it to glutamine or glutamate—is evolutionarily conserved. Since glutamine is a neurotoxin, however, mammals must further convert the excess amino acids to urea. “The root cause of ammonium toxicity is not understood in mammalian systems,” says Hess. At least now, he says, “we can use yeast as a model.”